These findings indicate that acquired resistance to T-cell–based immunotherapy that can occur in patients is not due to loss of target antigens or IFNγ signaling, which appear to remain intact, but rather to other mechanisms yet to be identified.

This study shows how common downregulation of a stress response gene in liver cancer promotes metastatic progression, also providing a mechanistic rationale for new therapeutic approaches in this setting.

These findings provide a rationale for targeting the arginine methyltransferase Prmt1, a regulator of protein translation, as a strategy to eradicate cancer cells, which commonly display unique translation-dependent requirements.

These findings provide new insights into epigenetic regulation of MYC function and suggest a novel pharmacologic basis to target histone demethylases as an indirect MYC-targeting approach for cancer therapy.

Drug resistance that arises invariably to cancer cell–targeted therapy also poses a challenge to antibody-drug conjugates, in this case through a novel mechanism involving alterations in the lysosome-based proteolytic activity.

These findings provide insights into how the interaction between LSD1 and SNAG domain proteins regulates transcription in neuroendocrine tumors and also offer a preclinical proof of concept for the therapeutic efficacy of targeting LSD1 in this setting.

This study shows how a signature of immune and desmoplastic stromal markers in an aggressive form of breast cancer can produce a simple ontology for gauging tumor heterogeneity and informing prognosis.